Abstract

Objective: In this research, we explored the molecular mechanism of proteinuria in glomerulosclerosis rats and the protective effects of ATRA.

Methods: This research set up three groups: SHO group, GS group, and ATRA group (15 mg/(kg d), Sigma, St. Louis, MO). The serum creatinine (Scr), urea nitrogen (BUN), and 24-h proteinuria were detected 12 weeks after administration of ATRA. The pathological and ultrastructure changes were observed under light microscope and transmission electron microscope. The protein expression of TGF-β1 and Col-IV in glomerulus was detected by immunohitochemistry method. The mRNA and the protein expression of glomerular TRPC6 were detected by RT-PCR and Western blot.

Results: In the rat model of GS, the expressions of TRPC6 were significantly elevated compared with the normal rat group; however, the use of ATRA down-regulated the expression of TRPC6 in the glomeruli and attenuated glomerulosclerosis and proteinuria. Scr and BUN were also improved by the treatment of ATRA.

Conclusions: Our results demonstrated that ATRA could ameliorate glomerulosclerosis and proteinuria in GS, which may be related to suppressed expression of TRPC6.

Details

Title
ATRA attenuate proteinuria via downregulation of TRPC6 in glomerulosclerosis rats induced by adriamycin
Author
Zhang, Lei 1 ; Chen, Xiu-Ping 2 ; He, Qin 2 ; Jiang, Ling 2 ; Yuan-Han, Qin 2 

 Department of Pediatric Nephrology, The First Affiliated Hospital of GuangXi Medical University, Nanning, China;; Department of Pediatric, Affiliated Hospital of Hebei University, Baoding, China 
 Department of Pediatric Nephrology, The First Affiliated Hospital of GuangXi Medical University, Nanning, China; 
Pages
266-272
Publication year
2018
Publication date
Nov 2018
Publisher
Taylor & Francis Ltd.
ISSN
0886022X
e-ISSN
15256049
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
3109042156
Copyright
© 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.